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Abstract
We have created a transgenic reporter for virus infection, and used it to study Nora virus infection in Drosophila melanogaster. The transgenic construct, Munin, expresses the yeast transcription factor Gal4, tethered to a transmembrane anchor via a linker that can be cleaved by a viral protease. In infected cells, liberated Gal4 will then transcribe any gene that is linked to a promoter with a UAS motif, the target for Gal4 transcription. For instance, infected cells will glow red in the offspring of a cross between the Munin stock and flies with a UAS-RFPnls transgene (expressing a red fluorescent protein). In such flies we show that after natural infection, via the faecal-oral route, 5–15% of the midgut cells are infected, but there is little if any infection elsewhere. By contrast, we can detect infection in many other tissues after injection of virus into the body cavity. The same principle could be applied for other viruses and it could also be used to express or suppress any gene of interest in infected cells.
Highlights
We have created a transgenic reporter for virus infection, and used it to study Nora virus infection in Drosophila melanogaster
A striking characteristic of the Nora virus infection is that the virus titre differs enormously between individual fruit flies that are kept in the same vial and the titres may vary from 102 up to 1010 viral genomes per fly[2,3]
The w; upstream activating sequence (UAS)-RFPnls; Munin reporter fly stock expresses red fluorescent protein tagged with a nuclear localisation signal (RFPnls), under the control of the Munin reporter
Summary
We have created a transgenic reporter for virus infection, and used it to study Nora virus infection in Drosophila melanogaster. Infected cells will glow red in the offspring of a cross between the Munin stock and flies with a UAS-RFPnls transgene (expressing a red fluorescent protein). Nora virus is a currently unclassified picorna-like virus that naturally infects the fruit fly Drosophila melanogaster[1].
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